Hydrogen sulfide post-conditioning preserves interfibrillar mitochondria of rat heart during ischemia reperfusion injury

详细信息    查看全文

• 作者：Shakila A. Banu ; Sriram Ravindran ; Gino A. Kurian
• 刊名：Cell Stress and Chaperones
• 出版年：2016
• 出版时间：July 2016
• 年：2016
• 卷：21
• 期：4
• 页码：571-582
• 全文大小：1,801 KB
• 刊物主题：Biomedicine general; Cell Biology; Biochemistry, general; Immunology; Cancer Research; Neurosciences;
• 出版者：Springer Netherlands
• ISSN：1466-1268
• 卷排序：21

文摘

Cardiac mitochondrial dysfunction is considered to be the main manifestation in the pathology of ischemia reperfusion injury, and by restoring its functional activity, hydrogen sulfide (Hb>2b>S), a novel endogenous gaseotransmitter renders cardioprotection. Given that interfibrillar (IFM) and subsarcolemmal (SSM) mitochondria are the two main types in the heart, the present study investigates the specific Hb>2b>S-mediated action on IFM and SSM during ischemic reperfusion in the Langendorff rat heart model. Rats were randomly divided into five groups, namely normal, ischemic control, reperfusion control (I/R), ischemic post-conditioning (POC), and Hb>2b>S post-conditioning (POC_Hb>2b>S). In reperfusion control, cardiac contractility decreased, and lactate dehydrogenase, creatine kinase, and infracted size increased compared to both normal and ischemic group. In hearts post-conditioned with Hb>2b>S and the classical method improved cardiac mechanical function and decreased cardiac markers in the perfusate and infarct size significantly. Both POC and POC_Hb>2b>S exerts its cardioprotective effect of preserving the IFM, as evident by significant improvement in electron transport chain enzyme activities and mitochondrial respiration. The in vitro action of Hb>2b>S on IFM and SSM from normal and I/R rat heart supports Hb>2b>S and mediates cardioprotection via IFM preservation. Our study indicates that IFM play an important role in POC_Hb>2b>S mediated cardioprotection from reperfusion injury.KeywordsHydrogen sulfideIschemic post-conditioningMyocardial ischemia reperfusionInterfibrillar mitochondriaSubsarcolemmal mitochondria